Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts: Gene/Protein Disease Symptom Drug Enzyme Compound   Target Concepts: Gene/Protein Disease Symptom Drug Enzyme Compound

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Query: EC:2.6.1.1 (aspartate aminotransferase)
21,665 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Anaesthesia was induced in 24 horses with xylazine and ketamine and maintained with halothane (12 cases) or enflurane (12 cases) in oxygen. Pulse rate, arterial blood pressure, arterial blood gas values, respiratory rate and tidal volume were measured at regular intervals during anaesthesia. Serial venous blood samples were taken for assay of glucose, urea, haemoglobin, packed cell volume, gamma glutamyl transpeptidase, aspartate aminotransferase, alanine aminotransferase and creatine kinase. Operating conditions and the horses' behaviour in the recovery period were also recorded. In the case of the group of horses receiving enflurane, difficulty was experienced maintaining anaesthesia deep enough for surgery. This group also displayed greater respiratory depression. There were no significant differences between arterial blood pressure values, or any of the haematological or biochemical parameters recorded in each group. Recovery from anaesthesia was significantly faster in horses receiving enflurane but less smooth. It was concluded that, although enflurane appeared to be safe in the horse, the respiratory depression and the unpleasant recovery did not make it a desirable alternative to halothane.
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PMID:Clinical anaesthesia in the horse: comparison of enflurane and halothane. 397 74

Effects of yohimbine on xylazine-pentobarbital anesthesia were evaluated in ponies. Five minutes after the IV injection of xylazine (1.1 mg/kg of body weight), pentobarbital sodium (12.7 mg/kg, IV) and additional xylazine (2.2 mg/kg, IM) were given and produced anesthesia in 12 ponies for 64.0 +/- 16.4 minutes (mean +/- SD) as well as immobilization for 89.8 +/- 34.2 minutes. Eleven ponies were given yohimbine (0.1 mg/kg, IV) 50 minutes after pentobarbital dosing. In these 11 ponies, durations of anesthesia and immobilization were shorter, 52.0 +/- 1.4 and 65.5 +/- 14.8 minutes, respectively. The xylazine-pentobarbital combination caused bradycardia that was reversed by yohimbine injection. Xylazine-pentobarbital produced a small, but steady, decrease of mean arterial blood pressure, which was compounded by yohimbine administration and was evident for approximately 2 minutes. Within a minute after yohimbine injection, the ponies' respiratory rate decreased and the length of inspiration and expiration and thoracic breathing increased. This lasted approximately 2 to 3 minutes and was followed by an increase in respiratory rate. The anesthesia also produced a decrease in PaO2 that gradually returned to base line in 12 control ponies, but was more pronounced in 11 ponies given yohimbine. The PaCO2, although remaining moderately high in control ponies, returned to base line after yohimbine injection. An increased pHa was seen 60 minutes after induction of anesthesia and was especially noticeable after yohimbine administration. Decreases in the number of WBC, hemoglobin content, PCV, plasma protein and serum aspartate transaminase resulting from xylazine-pentobarbital were reversed by yohimbine. Conversely, serum glucose values and creatine kinase activities were increased by xylazine-pentobarbital.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Antagonism of xylazine-pentobarbital anesthesia by yohimbine in ponies. 402 6

One hundred and forty-one randomly selected surgical patients, aged 35 years or over, were studied preoperatively, followed through their operative procedures, and reassessed during the first post-operative week for evidence of myocardial ischaemia associated with surgical operations under general anaesthesia. Of these patients 38% were found to have preoperative clinical evidence of heart disease, hypertension, or diabetes; 45% had abnormal preoperative E.C.G. patterns.Three patients experienced myocardial infarction during or within 36 hours of operation, all of the occult type; all were in the preoperative abnormal groups. Non-specific postoperative E.C.G. changes were equally common in the groups of patients with normal or abnormal preoperative electrocardiograms.A relationship existed between a rise in serum lactic dehydrogenase (L.D.H.) concentration and the field of the operation, but the diagnosis of infarction was not confused provided serum L.D.H. isoenzyme patterns and a rise in serum aspartate aminotransferase (S.G.O.T.) levels were consistent with the diagnosis.
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PMID:Myocardial infarction following surgical operations. 572 23

In 38 patients subjected to retropubic prostatectomy the effects of continuous lumbar epidural analgesia for 24 hours and the thiopentone- oxygen-nitrous oxide- alcuronium-pethidine sequence with artificial ventilation on the serum activities of aspartate aminotransferase (ASAT), alanine aminotransferase (ALAT), alpha-hydroxybutyrate dehydrogenase (HBD), and alkaline phosphatase (AP) have been studied. Per- and postoperative complications were recorded according to a prearranged plan designed to quantify the peroperative haemorrhage, postoperative deep vein thrombosis, pulmonary, circulatory and infectious complications. ASAT, ALAT and AP in the general group and ALAT in the epidural group showed significant increases on the 5th and 7th postoperative days. There existed no statistically significant difference between the groups. 82% of the patients with documented postoperative complications combined with hypoxaemia showed a pathologic liver enzyme pattern in contrast to 9% of the patients with uneventful postoperative course. It is concluded that the method of anaesthesia did not have an effect on the liver enzymes. Complications combined with postoperative hypoxaemia seemed to be the factors responsible for the increases of liver enzymes.
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PMID:Liver enzymes after retropubic prostatectomy in patients receiving continuous lumbar epidural analgesia or general anaesthesia. 618 33

Effects of halothane anesthesia were investigated in ponies prepared surgically with chronic external biliary fistulas (T tubes) to determine the effects on liver function and biliary excretion during 2 hours of anesthesia. Four studies were performed on 2 ponies, 2 to 6 months after surgery with the enterohepatic circulation held intact between studies. Intravenous bile acid infusion was used to maintain steady-state bile flow, bilirubin, and bile acid excretion during each study. Compared with the immediate 2-hour preanesthesia values (base line), halothane caused a 138% increase in bilirubin excretion, a 60% increase in biliary bilirubin concentration, and a 43% increase in PCV. Halothane anesthesia also caused a 16% reduction in plasma bilirubin, a 46% reduction in biliary bile acid concentration, and a 27% reduction in bile acid excretion. The bile acid independent fraction of bile flow appeared to increase. Plasma aspartate transaminase concentration did not change during anesthesia. The ratio of conjugated bilirubin fractions in bile [82% to 83% disconjugates of glucuronide and glucoside (2 forms) and 17% to 18% monoconjugates of glucoside, glucuronide, and xyloside] did not change during anesthesia and less than 1% was excreted unconjugated. Halothane anesthesia did not appear to affect adversely the activity of the transferase-conjugating enzymes in the presence of an increased bilirubin load. Seemingly, greatly increased conjugated bilirubin excretion observed during halothane anesthesia was most likely the result of a combination of increased hepatic clearance from plasma and increased hepatic bilirubin production from turnover of free hepatic heme or heme from the induced cytochrome P-450 system.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Effects of halothane anesthesia on equine liver function. 673 75

The acute 2-hour effects of isoflurane anesthesia on liver function and biliary excretion were examined in 2 ponies prepared surgically with chronic external biliary fistulas (T-tubes). Studies were conducted 2 to 8 months postoperatively with the enterohepatic circulation held intact between studies. Bile acid infusion IV (8.1 to 8.8 mumol/min) helped maintain bile flow and bile acid and bilirubin excretion during complete biliary diversion throughout each study. Following 3-hour control periods, anesthesia was induced and maintained at 1.3 to 1.5 minimal alveolar concentration plus O2 (spontaneous breathing) for 2 hours. Compared with the immediate 2-hour preanesthesia values, isoflurane caused significant increases in PCV (27%) and biliary bilirubin excretion (24%). However, no significant differences were detected in plasma or biliary bilirubin concentrations, biliary bile acid concentration or excretion, bile flow, or plasma aspartate aminotransferase concentrations between preanesthesia control and anesthesia periods. The results indicate that although isoflurane anesthesia enhanced hepatic bilirubin excretion, its effects on hepatic bilirubin formation and/or clearance are modest, compared with effects of halothane anesthesia which have previously been shown to enhance equine bilirubin excretion by 138% and reduce bile acid excretion by 27%. Isoflurane anesthesia in ponies does not appear to affect hepatic bile acid transport or bile formation significantly.
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PMID:Effects of isoflurane anesthesia on equine liver function. 673 76

The possible myotoxic effect of bupivacaine in combination with tourniquet ischemia was evaluated in 11 patients who underwent surgery of an arm under intravenous regional anesthesia. Eleven patients with the same kind of surgery and tourniquet who had general anesthesia served as controls. Venous blood bupivacaine concentrations in the anesthetized arm were high at the end of tourniquet time (27.2-202 micrograms/m1) and varied from 2.3 to 12.3 micrograms/ml 10 min after tourniquet release. Changes in blood-gas tensions and plasma potassium and lactate concentrations before and just after tourniquet release correlated with the ischemia time. Changes in creatine phosphokinase, lactate dehydrogenase and aspartate aminotransferase activities, possible indices of loss of integrity of muscle cell membranes, varied considerably and did not correlate with the ischemia time. There were no significant differences between the two groups in any of the parameters. Electron microscopy revealed no evidence of muscle degeneration 24 hr after the use of tourniquet with either bupivacaine intravenous regional (n = 4) or general anesthesia (n = 3).
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PMID:Evaluation of the myotoxicity of bupivacaine in bier blocks--a biochemical and electron microscopic study. 688 67

Intracompartmental muscle pressures were recorded from the right and left forelimbs (extensor carpi radialis, triceps brachii) of healthy horses maintained in left lateral recumbency while under deep halothane anesthesia for 180 to 240 minutes. Cardiac output, blood pressure, blood gases, and acid-base status were monitored throughout the anesthesia, and electrolyte levels (Ca2+, P+, K+, Cl-, Na+) and enzyme activities (aspartate aminotransferase (AST), creatine phosphokinase (CPK), and blood lactate) were monitored for 7 days. Postanesthetic forelimb lameness was produced in 5 of the 6 horses with this prolonged anesthetic regime. This lameness was associated with muscle plaque formation and clinical signs which were similar to the forelimb lameness sometimes seen in horses after surgical anesthesia. Plasma protein, serum calcium, plasma sodium, and blood urea nitrogen concentrations did not change, whereas significantly increased hematocrit, plasma potassium, and serum inorganic phosphate values were seen at the end of anesthesia, along with a decrease in plasma chloride values. Blood lactate, serum AST, and serum CPK activities were significantly high in the postanesthetic period, although the sequence of the changes differed. Intracompartmental muscle pressures were higher in the left forelimb adjacent to the floor (contact limb), and in the instance of the triceps of the contact limb, the pressures were sufficiently high (greater than 30 mm of Hg) that they may have compromised capillary blood flow. However, these high intracompartmental muscle pressures did not persist when positional changes of the horses were introduced at the end of the anesthetic period. There was no correlation between the severity of postanesthetic lameness and any of the measured values. The results demonstrate an experimentally induced postanesthetic lameness which was primarily related to the development of a myositis. Although the causative factors of this myositis may be multiple, the present study implicates local hypoxia in that increased blood lactate and inorganic phosphate values preceded that increased CPK activity. Intracompartmental muscle pressure in the contact limb were possibly high enough to have restricted local capillary blood flow.
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PMID:Equine postanesthetic forelimb lameness: intracompartmental muscle pressure changes and biochemical patterns. 721 25

The effects of different kinds of anesthesia on the function of live (evaluated on the basis of activity of enzymes -- aspartate aminotransferase, fructose-I-monophosphate aldelase and glutamate dehydrogenase) were studied in 63 infantile patients with Hodgkin's disease who underwent diagnostic laparotomy with splenectomy. It was found that during the first 6 days after surgery, the rate of activity of these enzymes shows a rise and reaches the upper limits in 77.8% of cases. Halothane anesthesia induced excessive enzymatic activity in 100%, while neuroleptanalgesia -- in 53.8% of cases. Repeated application of halothane produced a higher hepatotoxic effect as manifested by enhanced activity of glutamate dehydrogenase on days 1--2 after operation.
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PMID:[Effect of fluorothane anesthesia on liver function in children suffering from lymphogranulomatosis]. 724 73

Succinylcholine chloride administered to horses anesthetized with halothane in oxygen and mechanically ventilated, caused slight but statistically insignificant (P less than 0.01) increases in creatine phosphokinase, lactic dehydrogenase, and aspartate aminotransferase activity. The increases in these enzymes have been explained on the basis of muscle damage resulting from succinylcholine chloride induced muscle fasciculations and by hypoperfusion of tissues due to depression of the cardiovascular system caused by general anesthesia. These changes were not clinically apparent based upon the absence of myoglobinuria and ease of recovery. There was no significant effect of treatment observed on other biochemical variables. The findings in the present study agree with previous observations on serum creatine phosphokinase, lactic dehydrogenase, and aspartate aminotransferase activity.
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PMID:Biochemical effects of succinylcholine chloride in mechanically ventilated horses anesthetized with halothane in oxygen. 740 95


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